Asthma is a common chronic inflammatory disease in the airways. It was
thought to be caused by the combination of environment and genetic factors.
Previous studies have suggested that cell immunity played a vital role in
regulating the airway hyper reactivity (AHR) and inflammation. Fei Xu of the
First Affiliated Hospital of Nanchang University in China developed a mouse
model for asthma by expressing the human IL10 and TGFB1 genes to explore the
possible interaction between these two during asthma progression.

The transgenic mice exhibited enhanced expression of IL10 and TGFB1. During
the ovalbumin challenge, transgenic mice displayed a 1.9-fold higher MCh50
score than wildtype counterparts. Meanwhile, a three-fold decrease of cell
counts in bronchoalveolar lavage fluid (BALF) was also recorded. These
results suggested that IL10 and TGFB1 cooperatively protected the
respiratory system in response to antigenic stimulus.

To study the behaviors of these two genes, the team quantified the
expression of downstream genes in both IL10 and TGFB1 signaling. The
examined genes in IL10 signaling were significantly repressed, especially
IL5. Meanwhile, most genes were not altered in TGFB1 signaling.

These evidences proved that the activation of IL10 and TGFB1 protected the
host from ovalbumin-induced asthma, possibly through IL10 signaling. This
study shed some light on the modulations these two genes and related
networks to asthma progression.

[link.springer.com]